Anorexia nervosa (AN) is a serious mental illness characterized by reduced caloric intake that often persists after acute weight restoration. This preliminary study assesses the relationship between pre-meal anxiety and food intake in recently weight-restored individuals with AN. We hypothesized that pre-meal anxiety is inversely related to caloric intake in AN. Caloric intake and pre-meal anxiety were measured in three laboratory-based assessments (yogurt snack, multi-item lunch, macaroni and cheese lunch). Anxiety was measured by Spielberger State-Trait Anxiety Inventory (STAI-S) administered prior to the meal. Acutely weight-restored patients with AN were compared with healthy controls (HCs). Associations between anxiety and intake were analyzed first within each meal type separately and then using a model to combine the sample. In the multi-item lunch and the macaroni and cheese lunch, AN ate significantly less than HC (p = 0.01, p < 0.001). Pre-meal anxiety was significantly correlated with intake among AN, but not HC. In the yogurt snack, there was no significant association between anxiety and intake among patients or controls, and the groups did not differ in caloric intake. The association between pre-meal anxiety and intake among weight-restored individuals with AN suggests a potential target for relapse prevention treatment.
Anorexia nervosa (AN) is a serious psychiatric illness with a mortality rate among the highest of any psychiatric illness (Papadopoulos, Ekbom, Brandt, & Ekselius, 2009). Mortality increases over time, and is estimated to be 5% per decade of illness (Sullivan, 1995). The disorder is characterized by severe weight loss, body image distortions/overemphasis on shape and weight, and fear of “fat” or weight gain. Initial treatment focuses on restoring normal weight and structured behavioral treatment programs are generally successful in achieving this goal. However, the relapse rate after acute weight restoration is substantial, with as many as 50% of patients requiring re-hospitalization with in the year after discharge (Pike, 1998). Although many psychological symptoms improve with weight gain, often to within normal limits (Attia, Haiman, Walsh, & Flater, 1998), significant problems with food choice and caloric intake persist (Sysko, Walsh, Schebendach, & Wilson, 2005). Specifically, dietary choices made by weight-restored patients on an inpatient unit have been shown to be associated with outcome such that those who made food choices lower in energy density and diet variety, even with similar caloric intakes, were more likely to have a poor outcome in the year following discharge (Schebendach et al., 2008). Understanding the factors associated with the persistence of dysfunctional eating behavior after acute weight restoration may suggest novel targets for treatment.
The persistence of dysfunctional eating behaviors in individuals with AN may be related to anxiety (Steinglass et al., 2010). We recently proposed a model of AN linking eating behavior with anxiety. Baseline anxiety and obsessionality lead to fear of food, avoidance of food, and rigid dieting behavior. These factors interact and lead to weight loss. Weight loss in turn increases baseline anxiety and obsessionality and serves to perpetuate the cycle of dysfunctional eating behavior. In support of this model, a previous study by our group found that patients, even after weight restoration and improvement in many psychological symptoms, continued to significantly restrict their eating during a laboratory test meal (Sysko et al., 2005). A subsequent study demonstrated that repeated presentation of the same laboratory meal, with a therapist present for encouragement, led to increases in total intake (Steinglass et al., 2007). To begin to address the question of the relationship between pre-meal anxiety and food intake in weight-restored individuals with AN, we combined data from three ongoing studies that each include a laboratory-based eating assessment. We hypothesized that pre-meal anxiety would be inversely related to caloric intake among individuals with AN. As a preliminary test of this hypothesis, we examined each meal study separately and then pooled these data to create one model and thereby increase power to detect an effect.
